束支超常传导3例

在基本心搏呈持续性束支传导阻滞或显性预激时，期前收缩。出现间歇性QRS波群变窄的矛盾正常化现象。该现象可由窦性或室上性伴束支传导阻滞，也可预激并发期前收缩QRS波群正常化。其心电图特点及形成机制有多种，     

特殊类型QRS波正常化8例报告

QRS波形态正常化是指室上性或室性心律呈单侧束支传导阻滞或预激综合征(WPW)图形,而室性或非室性异位心律时,QRS形态正常或基本正常的一种心电现象,通常与期前收缩有关。本文分析8例特殊类型QRS波正常化,将其分类并探讨其发生机理。     

期前收缩的QRS波群正常化13例分析

期前收缩ＱＲＳ波群正常化现象 ,是指束支传导阻滞或典型预激综合征患者的期前收缩ＱＲＳ波群形态和时间反趋于正常 ,即基本心搏宽、期前收缩窄的矛盾现象 ［１ ,２］。该现象在心律失常鉴别诊断中具有重要价值 ,且偶尔出现的正常化心搏对某些被束支传导阻滞或预激综合征所掩盖的心电现象 (如心肌缺血等 )亦有揭示作用 ［３］。本文探讨该现象的心电图特点及形成机制。资料和方法以１９７３～２０００年本院４２４３０例常规心电图中符合以下条件的作为分析对象 :(１)基本心律为窦性心律 ,(２)有持续出现的束支传导阻滞或预激综合征 ,(３)有…     

表现为逸搏的室性并行收缩

患者男,60岁,临床诊断:冠心病。有完全性右束支传导阻滞史10年。心电图(附图)示窦性心律,P-P间期规则,心率72次/min。QRS波群形态有4种:(1)基本QRS波群为完全性右束支传导阻滞图形,(2)提前出现宽大畸形的QRS波群为室性期前收缩,(3)期前收缩后延迟出现的QRS波群颇似室性逸搏,呈左束支传导阻滞型,但“逸搏”无固定偶联间期,Ⅱa的R_9-R_(10)、Ⅱc的R_7-R_8和V_1导联的R_3-R_4是短的异位周期,间期为1.10s,其余的长异位周期是短周期的倍数,(4)窦性与“逸搏”冲动形成的室性融合波(F)。心电图诊断:窦性心律,完全性右束支传导阻滞,频发室性期前收缩,以逸搏形式表现的室性并行收缩(可能与右束支传导阻滞有关)。 讨论 通常所见逸搏的心电图表现为:逸     

双重性室性逸搏伴正常化的室性融合波群

患者男,68岁,因意识模糊、大小便失禁1天入院。有原发性高血压、冠心病史10余年。心电图(附图)见P波规律出现,频率115次/min,P波落于心动周期的不同时相,与QRS波群完全无关,为三度房室传导阻滞。QRS波群呈现3种形态:(1)完全性右束支传导阻滞(附图上行R_1、中行R_6、下行R_4);(2)完全性左束支传导阻滞型(附图上行R_(2、4、6)、中行R_(1—4)、下行R_(1、2、5、6);(3)中间型(附图上行R_(3、5)、中行R_5、下行R_3),形态时限正常。上述3种QRS波群间断出现,R-R基本规则,频率58—65次/min,考虑为加速性室性逸搏心律,右束支传导阻滞型QRS波群提示冲动源于左心室,左束支传导阻滞型则来自右心室,形态正常的QRS波群为前二者同步激动心室所致的正常化室性融合波群。心电图诊断:窦性心律,双重加速型室性逸搏心律伴正常化的室性融合波群,三度房室传导阻滞。     

早搏QRS波群正常化心电图四例分析

早搏QRS波群正常化,是指伴有单侧束支阻滞或预激综合征的室上性激动并发室性或室上性早搏时,早搏的QRS波群形状与时限反趋于正常,即基本心律QRS波群宽,而早搏QRS波群窄的矛盾现象。该现象由Massumi等首先报道。国内曾有个案报告,现将     

早搏QRS波群正常化

早搏QRS波正常化(简称早搏QRS正常化),是指伴有束支阻滞(BBB)或WPW综合征者在并发室上性或室性早搏(室早)时,早搏QRS形状与时间反趋于正常。即基本心律QRS波宽,早搏QRS波窄的矛盾现象。 一、窦性(或室上性,下略)心律伴BBB时并发早搏QRS正常化 1、窦-室室性融合波(VF):源于患侧束支同侧的舒张晚期室早与窦性经健侧束支下传共同激动心室。     

房颤时QRS宽与窄的矛盾现象

房颤时,f波冲动下传心室过程中,由于室内束支传导阻滞或者冲动经房室旁道下传,形成的QRS是宽型(即束支阻滞型或预激型),这是房颤心律下基本形态的QRS。在上述图形的基础上,夹有窄型的QRS(即QRS“正常化”),这种“正常化”QRS有的是早发的,有的迟发的。此则构成了一种心电矛盾现象。     

逸搏QRS波群正常化

伴有单侧束支阻滞的窦/房性激动,并发房室传导阻滞而出现逸搏时,其QRS波群的形态及时限反而正常(或趋于正常),称为逸搏QRS波群正常化。该现象亦称窦/房性心律QRS宽而逸搏心律QRS窄的矛盾现象。简治芳等(1983)曾报道1例。现将我们遇到的3例报告如下。 例1 女,35岁。临床诊断:心肌炎。ECG(图     

《思考心电图之132》答案

窦性P-P间期0.80~0.84s,频率71~75次/min, QRS波群呈典型完全性右束支传导阻滞图形（时间0.13s）,其前均有低小心室起搏脉冲出现,P-R（V）间期固定为0.16s,且不以P-P间期的长短而改变,呈现“窦性P波-心室起搏脉冲-完全性右束支传导阻滞型QRS波群”,强烈提示该起搏器为双腔起搏器（心室为双极起搏）,心房电极感知窦性P波后通过设置的P（A）-V间期触发心室发放脉冲,呈现VAT起搏模式。形成这种QRS波群有以下3种可能：（1）窦性心律、完全性右束支传导阻滞、伪室性融合波群：即该QRS波群由窦性P波顺传,存在完全性右束支传导阻滞,心室起搏脉冲与QRS波群无关,仅重叠在QRS波群起始部形成伪室性融合波群,此种可能性最大。（2）心室起搏脉冲引发心室起搏形成该QRS波群：一般情况下,双腔起搏器的心室电极大多植入在右心室的心尖部,引发心室除极所形成的起搏QRS忆波群呈类左束支传导阻滞图形;当其起搏电极穿过室间隔植入左心室心内膜或误入冠状静脉的侧静脉所引发心室除极时,可形成类右束支传导阻滞图形QRS波群,但V1绝不会出现典型的三相波（rsR忆型）,此种可能性极小。（3）窦性心律、完全性右束支传导阻滞、室性融合波群：即窦性激动与心室起搏激动共同除极心室形成真性室性融合波群,但以窦性激动控制心室为主;从P-R（V）间期固定,且不以P-P间期的长短而改变及QRS波群呈典型完全性右束支阻滞图形看,此种可能性较小。〈br〉 综上所述,本例心电图诊断为：（1）窦性心律;（2）完全性右束支传导阻滞;（3）双腔起搏器,以VAT模式工作,其心房感知功能正常,而心房和起搏功能及心室感知功能未能评价;（4）伪室性融合波群。     

Interventricular septal motion during preexcitation and normal conduction in Wolff-Parkinson-White syndrome: echocardiographic and electrophysiologic correlation.

Interventricular septal motion was studied by echocardiogram in 20 consecutive patients with documented Wolff-Parkinson-White (WPW) syndrome before and during electrophysiologic evaluation using His bundle recordings and pacing techniques. Characteristic abnormal interventricular septal motion was seen in 8 of 11 patients with type B WPW syndrome (groups I and II). All eight patients had electrocardiographic patterns consistent with an anomalous pathway located in the anterior right ventricular wall (group I). In five of these eight patients normalization of the QRS complex for one or more beats was accomplished and produced normalization of the septal motion in four; whereas in the fifth patient, who had an underlying atrial septal defect, the abnormal septal motion remained abnormal. All nine patients with type A WPW syndrome (groups III to V) had normal septal motion both during total preexcitation and during normalization of the QRS complex. The normalization of the abnormal interventricular septal motion with normalization of the QRS complex in type B WPW syndrome strongly suggests that the abnormal motion is related to an abnormal sequence of ventricular depolarization during preexcitation. Furthermore, persistent abnormal septal motion after normalization of the QRS complex suggests that other factors such as right ventricular volume overload may be responsible. Likewise, when abnormal septal motion occurs in the presence of type A WPW syndrome, an explanation other than preexcitation must be sought.     

Familial atrioventricular heart block; an autosomal dominant trait.

A family of 28 individuals spanning four generations was investigated because of a finding of complete heart block in five members and the existence of a low degree of atrioventricular (A-V) heart block in a sixth member. The disorder was characterized by 1) adult onset in all, 2) complete A-V heart block in five and first degree A-V heart block in one, 3) sinus bradycardia in three, 4) atrial fibrillation in five, 5) abnormal QRS complex in five, 6) ventricular tachycardia in three, 7) left ventricular enlargement in all, and 8) mitral insufficiency in five. Proximal location of the A-V heart block was suggested by the fact that atropine caused acceleration of the ventricular rate and by the presence of a His bundle potential preceding the QRS complexes. Involvement of the distal conducting system was indicated by the widened QRS complex and a prolonged H-V interval. Pathologic examination in one case showed extensive sinus node fibrosis and interruption of the A-V node-His bundle connection. This disorder is probably due to an autosomal dominant trait.     

Cardiac memory during rather than after termination of left bundle branch block

An 83-year-old woman with chronic left bundle branch block and remote history of pacemaker implantation for intermittent AV block was hospitalized for fatigue and leg swelling. She had no cardiac complaints. Routine 12-lead electrocardiogram showed sinus rhythm with left bundle branch block. There were diffuse negative T waves in the inferior and anterolateral leads that were concordant with the QRS complexes. Echocardiogram was normal and nuclear perfusion heart scan showed no abnormality. It was noted that the negative T waves during left bundle branch block were in the exact same leads as were the deep negative QRS complexes during ventricular pacing. The electrocardiographic changes were consistent with cardiac memory. This case is unique because cardiac memory in patients with intermittent left bundle branch block typically occurs when the QRS complexes normalize and not during left bundle branch block itself. Our findings indicate that memory Ts can develop not only after normalization of wide complex rhythms but also with alternating wide complex rhythms as in the presented case where a ventricular paced rhythm was replaced by left bundle branch block.     

Bundle branch block. Demonstration of the incomplete nature of some "complete" bundle branch and fascicular blocks by the extrastimulus technique

The incomplete nature of some electrocardiographic “complete” bundle branch and fasclcular blocks is demonstrated using the atrial extrastimulus technique. Patient 1, with a QRS pattern of “complete” left bundle branch block, manifested a QRS pattern of right bundle branch block at a shorter coupling interval, indicating that the left bundle could conduct. Patient 2, with a QRS pattern of right bundle branch block and “complete” left anterior hemiblock, manifested a pattern of left posterior hemiblock at a shorter coupling interval, indicating that the left anterior fascicle could conduct. Patient 3, with a normal QRS complex, showed left bundle branch block at shorter coupling intervals and then a pattern of right bundle branch block as the coupling interval was further decreased, indicating that functional left bundle branch block was incomplete. This demonstration of partial bundle branch block depends on a discordance of conduction time and refractory period, the bundle or fascicle with depressed conduction (incomplete block) having a shorter refractory period than the more normally conducting bundle or fascicle. This discordance may be related to the development of trifascicular block in patients with bifascicular block and a normal H-V interval. It is a predisposing factor in the complex patterns of aberrant conduction seen during supraventricular tachyarrhythmias with varying cycle lengths.     

Wide complex tachycardia with atrioventricular dissociation and QRS morphology identical to that of sinus rhythm: a manifestation of bundle branch reentry.

OBJECTIVE: To determine the features that distinguish bundle branch reentry (BBR) ventricular tachycardia from a supraventricular tachycardia with aberration on the 12 lead electrocardiogram (ECG). PATIENTS: Three patients in whom premature beats (2 cases) or sustained tachycardia (2 cases) showed a QRS configuration identical to that observed during sinus rhythm. INTERVENTIONS: Programmed electrical stimulation. RESULTS: These arrhythmias were ventricular in origin and caused by a BBR mechanism, as suggested by the following data obtained during electrophysiological study: (a) an H-V interval shorter during tachycardia than during sinus rhythm; (b) A-V dissociation; (c) activation of the right bundle branch before activation of the bundle of His. The ECG of all 3 patients showed right bundle branch block with very prolonged QRS duration (0.16 to 0.20 s). Characteristically, all 3 had prolonged H-V interval during sinus rhythm. All patients had had a previous myocardial infarction and had a dilated left ventricle. CONCLUSION: The presence of (a) wide complex extrasystoles or tachycardia with a QRS morphology identical to that of sinus rhythm; (b) A-V dissociation; and (c) a very prolonged QRS duration (0.16 s or more) is suggestive of ventricular tachycardia caused by bundle branch reentry.     

Intracardiac electrode catheter recordings of atrioventricular bypass tracts in Wolff-Parkinson-White syndrome: techniques, electrophysiologic characteristics and demonstration of concealed and decremental propagation

Atrioventricular bypass tract deflections were recorded in five patients with the Wolff-Parkinson-White syndrome using standard, closely spaced (5 mm) electrode catheters. Three right paraseptal and two left-sided Kent bundles were recorded at the level of the tricuspid valve on the His bundle catheter and in the coronary sinus, respectively. Characteristics of the bypass tracts were studied during atrial pacing, programmed premature atrial stimulation, induction of supraventricular tachycardias and programmed ventricular stimulation. During atrial pacing, as pre-excitation increased, the stimulus to bypass tract deflection time remained unchanged. In five patients normalization of the QRS complex coincided with loss of the bypass tract deflection during incremental atrial pacing. Two patients demonstrated fragmentation of the bypass tract deflection before block. In one patient fragmentation of the bypass deflection coincided with normalization of the QRS complex. The effective refractory periods of the bypass tracts coincided with loss of bypass tract deflections in three of the five patients. In one patient, the effective refractory period of the bypass tract at its ventricular insertion preceded that at its atrial insertion, whereas in the remaining patient, the effective refractory period of the bypass tract was not attained because of atrial refractoriness. During orthodromic supraventricular tachycardia, the bypass tract deflections disappeared in the anterograde limb in all patients. In one patient, the bypass tract deflection was recorded during atrial fibrillation with pre-excitation. In conclusion: Bypass tract deflections can be recorded with a closely spaced electrode catheter. Right paraseptal bypass tracts are located close to the His bundle. The anterograde effective refractory period of the bypass tract usually reflects its atrial insertion, but concealment through the bypass tract can occur with block at the ventricular insertion. Decremental conduction within the bypass tract can occur before block, suggesting concealed and overt Wenckebach block within the bypass tract. Recordings of bypass tract deflections increase the potential of closed chest ablation of right paraseptal and left-sided bypass tracts.     

Mechanisms of regular,wide QRS tachycardia in infants and children

A regular, wide QRS tachycardia was electrocardiographically documented in 32 patients aged 1 month to 18 years. The mechanisms of the tachycardia were evaluated using standard multicatheter electrophysiologic techniques. These mechanisms included (1) orthodromic reciprocating tachycardia with bundle branch aberration (seven patients), (2) antidromic reciprocating tachycardia using single (three patients), or multiple (three patients) atrioventricular connections (Kent bundles), (3) atrial flutter with ventricular preexcitation over accessory connections (eight patients), (4) reciprocating tachycardia using a nodoventricular connection (Mahaim fiber) (five patients), and (5) ventricular tachycardia (six patients). Regular, wide QRS tachycardias are not rare in pediatric patients. Their mechanisms can be quite complex, and electrocardiographic analysis with respect to QRS configuration, heart rate, or the presence or absence of ventriculoatrial dissociation is not sufficient for diagnostic purposes. Our results show that considerable understanding of the mechanism of regular, wide QRS tachycardias can be obtained by multicatheter electrophysiologic study. Understanding the mechanism is essential in order to make rational use of available therapeutic options.     

Supernormal Conduction in the Left Bundle Branch

Supernormal Conduction. This report describes a patient with tachycardia-dependent left bundle branch block (LBBB) and atrial extrasystoles, some of which were followed by an unexpectedly narrow QRS complex. His-bundle recordings and premature atrial stimulation were performed to analyze the mechanism underlying the normalized intraventricular conduction of some of the early atrial impulses. The results suggested the presence of supernormal conduction in the left bundle branch (LBB), because(1) the HV interval was identical in LBBB complexes and in early narrow QRS complexes; (2) during single lest stimulation using different paced atrial cycle lengths, there was a well-defined range of H₁, H₂, intervals resulting in normalization of intraventricular conduction; and (3) atrial pacing with a cycle length of 500 msec resulted in alternation between wide and narrow QRS complexes. These findings rule out alternative mechanisms that could explain the unexpectedly normal intraventricular conduction of early impulses.     

Longitudinal dissociation of the bundle of His and infra-His block

A case with advanced supra-His block and escape pacemaker at the proximal His block with longitudinal dissociation of the bundle of His is presented. These alterations caused a complete left bundle branch block and prolonged HV interval obtaining the normalization of the QRS after distal His extrasystole. We comment on the differential diagnosis between first degree intra-His and infra-His blocks.     

Effects of right bundle branch block on the antidromic circus movement tachycardia in patients with presumed atriofascicular pathways

BACKGROUND: The typical and most common tachycardia in patients with atriofascicular pathways is a macro reentrant tachycardia, with anterograde conduction over the decrementally conducting bypass tract and retrograde conduction over the right bundle branch-His-AV node axis resulting in a short V-right bundle branch and short V-H interval. OBJECTIVES: To report on changes in rate and QRS configuration when right bundle branch block (RBBB) develops spontaneously during antidromic tachycardia using an atriofascicular fiber. METHODS: Three of 25 patients with an antidromic circus movement tachycardia using a right-sided atriofascicular pathway showed episodes of right bundle branch block (RBBB) during ventriculo-atrial conduction. Effect of retrograde RBBB on tachycardia rate and QRS configuration was studied using intracardiac and extracardiac recordings. RESULTS: All 3 patients showed prolongation of their V-A interval when retrograde RBBB occurred during tachycardia, resulting in a longer tachycardia cycle length. The VA time increase ranged from 85 to 100 msec, with a mean 346 +/- 5 msec. Two of the 3 patients also showed a change in QRS configuration due to a more leftward shift of the frontal plane QRS axis. CONCLUSION: Rate changes in antidromic tachycardia in patients with atriofascicular fibers can be based on a shift in VA conduction from one bundle branch to the other. This may be accompanied by changes in the frontal plane QRS axis because of a change in ventricular activation sequence.